Effect of hypoxic and carbon monoxide-induced hypoxia on regional myocardial segment work and O2 consumption

The purpose of this study was to investigate the potentially greater responses of regional myocardial work and O2 consumption to hypoxic hypoxia than to CO-induced hypoxia. Twenty open-chest anesthetized dogs were studied under control and four hypoxic conditions, hypoxic hypoxia induced with either 8% O2 (SaO2=56%) or 6% O2 (SaO2=40%) gas mixtures, or CO-induced hypoxia produced by a 1% CO gas mixture for either 7 min (SaO2=67%; SaCO=30%) or 20 min (SaO2=40%; SaCO=56%). Ultrasonic crystals and a force gauge were utilized to measure myocardial shortening and force. Regional myocardial segment work was calculated by integrating myocardial segment shortening multiplied by its corresponding force. Radioactive micropheres were used to measure regional coronary blood flow during each condition. Transmural biopsies were utilized to measure arterial and venous O2 saturation with a four-wavelength microspectrophotometric method. Regional O2 extraction and consumption were calculated Regional coronary blood flow (77±38 ml/min per 100 g, control) increased with severe hypoxic hypoxia (293±206) and CO-induced hypoxia (150±128). Regional myocardial O2 extraction was decreased with both hypoxic and CO hypoxia. Regional myocardial O2 consumption was maintained even with severe hypoxic and CO hypoxia. Regional myocardial segment work/min increased from 343±205 g*mm/min with increasing levels of hypoxic hypoxia (564±677) and decreased with increasing levels of CO hypoxia (169±111). Regional segment work increased with increasing levels of hypoxic hypoxia and decreased with increasing CO hypoxia. The differential effects on segment work caused by the two types of hypoxia may be due to direct metabolic or autonomic differences.